Microbiologic characteristics, serologic responses, and clinical manifestations in severe acute respiratory syndrome, Taiwan.
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ABSTRACT:
SUBMITTER: Hsueh PR
PROVIDER: S-EPMC3016775 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The entire spectrum of diagnostic testing, from reagent supply to test performance, has been a major focus during the coronavirus disease 2019 (COVID-19) pandemic. The hope for serologic testing is that it will provide both epidemiologic information about seroprevalence as well as individual information about previous infection. This information is particularly helpful for high-risk individuals who may be outside of the viral shedding window, such as children with suspected multisystem inflammatory syndrome. It is not yet understood whether serologic testing can be interpreted in terms of protective immunity. These concerns must be addressed using highly sensitive and specific tests.
| S-EPMC7414299 | biostudies-literature
Project description:BACKGROUND:In 2003, Taiwan experienced a series of outbreaks of severe acute respiratory syndrome (SARS) and 1 laboratory-contamination accident. Here we describe a new phylogenetic analytical method to study the sources and dissemination paths of SARS-associated coronavirus (SARS-CoV) infections in Taiwan. METHODS:A phylogenetic analytical tool for combining nucleotide sequences from 6 variable regions of a SARS-CoV genome was developed by use of 20 published SARS-CoV sequences; and this method was validated by use of 80 published SARS-CoV sequences. Subsequently, this new tool was applied to provide a better understanding of the entire complement of Taiwanese SARS-CoV isolates, including 20 previously published and 19 identified in this study. The epidemiological data were integrated with the results from the phylogenetic tree and from the nucleotide-signature pattern. RESULTS:The topologies of phylogenetic trees generated by the new and the conventional strategies were similar, with the former having better robustness than the latter, especially in comparison with the maximum-likelihood trees: the new strategy revealed that during 2003 there were 5 waves of epidemic SARS-CoV infection, which belonged to 3 phylogenetic clusters in Taiwan. CONCLUSIONS:The new strategy is more efficient than its conventional counterparts. The outbreaks of SARS in Taiwan originated from multiple sources.
| S-EPMC7199491 | biostudies-literature
Project description:BackgroundPaediatric inflammatory multisystem syndrome (PIMS) temporally associated with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) (PIMS-TS) is a rare clinical syndrome associated with a multiorgan system dysfunction, especially acute cardiac injury, and mandates a higher level of care.Aim of reviewTo investigate cardiac manifestations, treatment characteristics, and outcomes of PIMS-TS.Key scientific concepts of reviewTwenty-six studies were included with 1228 pooled subjects, with a mean age of 8.6 years, which were dominated by male gender (53%), and African ethnicity (31%). 732 (38%) patients were reactive on a serological test, and 457 patients (45%) were positive on SARS-CoV-2 RT-PCR. ST-segment abnormalities were the most common ECG findings (16%, n/N: 34/212). Various markers of troponin and the pooled mean of BNP and NT-pro-BNP levels were elevated. Cardiomegaly and pericardial effusion (21.8%, n/N: 164/751) were the most common chest X-ray findings. In echocardiography, the majority of patients' left ventricular ejection fraction was reduced (59.0%, n/N: 180/305), with pericardial effusion/ pericarditis seen the most (17.44%, n/N: 221/1267), and Z score ≥ 2 in 28% (n/N: 42/139). Cardiac MRI findings were consistent with acute myocarditis. Intravenous immunoglobulin, corticosteroids, and vasoactive drugs were frequently utilized. The mean length of stay was 6 days, with most patients (71%, n/N: 834/1163) were admitted to the ICU. However, the overall prognosis was favorable, with 98% alive (n/N: 1235/1260), and more than 50% of patients experienced recovery of left ventricular systolic functions at discharge (116 out of 206 patients).
| S-EPMC7871802 | biostudies-literature
Project description:Summary backgroundThe coronavirus 2019 pandemic was caused by a new single-strand RNA virus that originated from Wuhan, China, and infected more than 190 countries. The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) coinfection with tuberculosis posed a serious public health concern and complicated the prognosis and treatment of patients. Since both are respiratory diseases, the sign and symptoms may overlap and could have synergistic effects on the host that can increase mortality during coinfection. The present investigation reported the clinical characteristics of patients having coinfection of COVID-19 and tuberculosis (COVID-TB).MethodsWe performed a retrospective investigation on COVID-19 infection in tuberculosis patients between the years 2020 and 2021. The SARS-CoV-2 was confirmed by PCR and the COVID-TB epidemiological and clinical findings were recorded on the day of admission and followed up for 25 days.ResultsThe mean age of the COVID-19 patients was 50 ± 15 years, 76.36% were male and 23.64% were female. Weight loss, sore throat, whooping cough, chest pain, and vomiting were common symptoms, and asthma, diabetes, arthritis, and hypertension were found as co-morbidities in COVID-TB. The D-dimer, lactate dehydrogenase, C-reactive protein, erythrocyte sedimentation rate, and creatine kinase levels increased 14-fold, 12.5-fold, 11-fold, 10-fold, and 7-fold respectively during COVID-TB. The patients suffered from hyperferritinemia and lymphocytopenia which increased the likelihood of death. The levels of D-dimer, lactate dehydrogenase, C-reactive protein, erythrocyte sedimentation rate, and creatinine kinase were positively correlated with patient age. The chest radiograph showed the infectious agents have consolidated opacity and peripheral dissemination in the lungs.ConclusionTuberculosis coinfection augmented the severity of COVID-19 and the likelihood of death, and high vigilance is recommended for respiratory pathogens in COVID-19.
| S-EPMC9985913 | biostudies-literature
Project description:Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo [1,2]. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE, with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigarcin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a meassure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE. We used Affymetrix microarrays (Human Genome U133 plus 2.0) to compare global gene expression between SARS-CoV-infected, mock-infected and SARS-CoV-ΔE-infected cells. For ech type of sample three hybridizations were carried-out (independent biological replicates).
2012-06-20 | E-GEOD-30589 | biostudies-arrayexpress
Project description:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly throughout the world, causing severe morbidity and mortality. Since the first reports of Coronavirus disease 2019 (COVID-19) in late 2019, research on the characteristics of specific humoral immunity against SARS-CoV-2 in patients with COVID-19 has made great progress. However, our knowledge of persistent humoral immunity to SARS-CoV-2 infection is limited. The existence of protective immunity after infection will affect future transmission and disease severity. Therefore, it is important to gather knowledge about the kinetics of antibody responses. In this review, we summarize the information obtained so far on the characteristics and kinetics of the SARS-CoV-2 infection of specific humoral immune response, especially in neutralizing antibodies and their relationship with disease severity. In addition, with the emergence of variants of concern, we summarize the neutralizing effect of specific humoral immunity on variants of concern after the initial SARS-CoV-2 infection and vaccination.
| S-EPMC9389018 | biostudies-literature
Project description: Not available
| S-EPMC5137839 | biostudies-literature
Project description:Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo [1,2]. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE, with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigarcin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a meassure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.
2012-06-21 | GSE30589 | GEO
Project description:Since early March 2003, the severe acute respiratory syndrome (SARS) coronavirus (CoV) infection has claimed 346 cases and 37 deaths in Taiwan. The epidemic occurred in two stages. The first stage caused limited familial or hospital infections and lasted from early March to mid-April. All cases had clear contact histories, primarily from Guangdong or Hong Kong. The second stage resulted in a large outbreak in a municipal hospital, and quickly spread to northern and southern Taiwan from late April to mid-June. During this stage, there were some sporadic cases with untraceable contact histories. To investigate the origin and transmission route of SARS-CoV in Taiwan's epidemic, we conducted a systematic viral lineage study by sequencing the entire viral genome from ten SARS patients. SARS-CoV viruses isolated from Taiwan were found closely related to those from Guangdong and Hong Kong. In addition, all cases from the second stage belonged to the same lineage after the municipal hospital outbreak, including the patients without an apparent contact history. Analyses of these full-length sequences showed a positive selection occurring during SARS-CoV virus evolution. The mismatch distribution indicated that SARS viral genomes did not reach equilibrium and suggested a recent introduction of the viruses into human populations. The estimated genome mutation rate was approximately 0.1 per genome, demonstrating possibly one of the lowest rates among known RNA viruses.
| S-EPMC356986 | biostudies-literature
Project description:Severe acute respiratory syndrome (SARS) is a new human disease caused by an animal coronavirus that adapted to efficient human-to-human transmission. The disease first emerged in November 2002 in Guangdong Province, China and spread globally within months. The SARS coronavirus (SARS CoV) affects multiple organ systems with severe viral pneumonia as its main clinical manifestation but with diarrhea, lymphopenia, and mild liver dysfunction being common extra-pulmonary manifestations. Increasing age and the presence of underlying respiratory diseases worsens the prognosis. Unlike other respiratory viral infections, transmission of SARS was less frequent in the first 5 days of illness and correlated with low viral load in the upper respiratory tract at this stage of the illness. This fortuitous feature of the disease allowed the public health measures of case detection and patient isolation to interrupt virus transmission in the community and abort the SARS outbreak. Bats are a reservoir of a virus closely related to SARS CoV and this may be the likely precursor from which the human-adapted SARS CoV emerged. Small mammals such as ‘civet-cats’ (Paguma larvata) within live animal markets in southern China serve as amplifiers of infection and these markets were the likely interface where zoonotic transmission occurred. The viral spike protein is necessary and sufficient for inducing protective antibody responses and has been a key target in the development of candidate vaccines.
| S-EPMC7149687 | biostudies-literature